Many polyps and dysplastic lesions in ulcerative colitis have phenotypic changes (blood group antigen, cytokeratins, CEA, TAG-72.3 antigen expression) and genetic changes (c-K-ras mutation, enhanced c-myc expression and pp60c-src activity) which are characteristic of invasive cancers.
Many polyps and dysplastic lesions in ulcerative colitis have phenotypic changes (blood group antigen, cytokeratins, CEA, TAG-72.3 antigen expression) and genetic changes (c-K-ras mutation, enhanced c-myc expression and pp60c-src activity) which are characteristic of invasive cancers.
Many polyps and dysplastic lesions in ulcerative colitis have phenotypic changes (blood group antigen, cytokeratins, CEA, TAG-72.3 antigen expression) and genetic changes (c-K-ras mutation, enhanced c-myc expression and pp60c-src activity) which are characteristic of invasive cancers.
197 patients with UC and 302 with CD (499 with inflammatory bowel disease (IBD] whose disease started before age 20 years and whose age at time of study was less than 25 years were investigated, with two age- and sex-matched controls for each patient.
CRH messenger (m) RNA was also examined in biopsy specimens of ulcerative colitis by the reverse transcribed polymerase chain reaction method and by in situ hybridisation.
The high intensity of CD44v6 and v3 epitope expression on crypt epithelial cells in ulcerative colitis suggests that CD44 isoforms may have an important role in ulcerative colitis.
In order to study if the IL-1 beta gene polymorphism might participate synergistically with the IL-1Ra gene polymorphism in susceptibility to UC and CD, individuals were distributed into carriers and non-carriers of allele 2 of the genes encoding IL-1 beta and IL-1Ra, in each of the patient groups and controls.
In order to study if the IL-1 beta gene polymorphism might participate synergistically with the IL-1Ra gene polymorphism in susceptibility to UC and CD, individuals were distributed into carriers and non-carriers of allele 2 of the genes encoding IL-1 beta and IL-1Ra, in each of the patient groups and controls.
Three p53 DNA polymorphisms (BstU I and Msp I restriction fragment length polymorphisms (RFLPs) in exon 4 and intron 6 respectively, and a 16 bp duplication in intron 3) and their haplotype combinations were studied in patients with colorectal cancer and compared with patients with ulcerative colitis and healthy controls.
Three p53 DNA polymorphisms (BstU I and Msp I restriction fragment length polymorphisms (RFLPs) in exon 4 and intron 6 respectively, and a 16 bp duplication in intron 3) and their haplotype combinations were studied in patients with colorectal cancer and compared with patients with ulcerative colitis and healthy controls.
Because the codon 241 polymorphism is in a functionally important domain III of ICAM-1, we may have identified an actual responsible genetic variation for genetically heterogeneous subsets of both UC and CD.
These observations suggest that the presence of Gly-86 in the HLA beta-chain and surrounding amino acid sequence of HLA-DRB1*1502 is strongly associated with susceptibility to UC.
DRB1*1501 and DRB1*1502 differ in only one amino acid at residue 86 (valine vs glycine), and 66% of the UC patients carried two glycines at position 86 in the HLA-DR beta-chain (vs 51% of control; P < 0.05).
After topical IL-10 enema treatment of three steroid therapy-refractory patients with ulcerative colitis, in vitro release of proinflammatory cytokines from IBD peripheral monocytes as well as LPMNC is dramatically down-regulated.
Predominant expression of the V delta 1 subtype was demonstrated in the small intestine of patients with coeliac disease and in the inflamed colon of patients with inflammatory bowel diseases (IBD: ulcerative colitis and Crohn's disease) as well as in colon biopsies taken from macroscopically normal areas of colon.
In the case of interleukin-2 knockout mice, the lesion restricted to the colon, is virtually identical to ulcerative colitis in humans, and is initiated by the normal bacterial flora.
In both ulcerative colitis and controls, expanded cells were constituted largely by T-cell receptor alpha beta+, CD4+, CD45RA- (helper), and CD8+, CD11b- (cytotoxic) phenotypes.
Based on this method, p53 overexpression occurs frequently in UC-associated carcinomas regardless of stage and pathological characteristics, in noncancerous dysplastic masses with high grade dysplasia, and in dysplasias of all grades situated adjacent to carcinomas.